Article Abstract

Abstract

In-stent restenosis (ISR), defined as a ≥50% reduction in coronary lumen diameter within the stent or within 5 mm of the stent edges, remains a relevant issue in the field percutaneous coronary intervention (PCI) (1). As first iteration in PCI, balloon angioplasty presented several drawbacks, including intimal and media dissection, abrupt vessel occlusion, late structural remodeling and, importantly, diffuse proliferative neointimal response due to traumatic vessel injury, resulting in a rate of restenosis greater than 40% (2). The introduction of coronary stents substantially improved procedural success and clinical outcomes after PCI by significantly reducing the risk of restenosis and nearly eliminating the risk of acute vessel closure with the consequent need for surgical standby (2). However, the lack of antiproliferative drug release from bare metallic platforms remained associated with higher rates of ISR and target vessel revascularization.